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Cardiology > Pharm. of Drugs Affecting Arrhythmias > Flashcards

Pharm. of Drugs Affecting Arrhythmias Flashcards

0
Q

In the Singh-Vaughan Williams classification scheme, what do class II drugs do?

A

Class II are beta-blockers

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1
Q

In the Singh-Vaughan Williams classification scheme, what do class I drugs do?

A

Block Na+ channels (local anesthetics) - slow conduction velocity and reduce excitability.

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2
Q

In the Singh-Vaughan Williams classification scheme, what do class III drugs do?

A

Class III drug are K+ channel blockers: prolong refractoriness, but don’t reduce excitability.

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3
Q

In the Singh-Vaughan Williams classification scheme, what do class IV drugs do?

A

Class IV drugs are Ca++ channel blockers (L-type Ca++ channels)

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4
Q

In the Singh-Vaughan Williams classification scheme, what do class IA drugs do?

A

block both Na+ and K+ channels

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5
Q

Name 1 class IA drug to remember?

A

Procainamide

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6
Q

Name 1 class IB drug to remember?

A

Lidocaine

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7
Q

Name 1 class IC drug to remember?

A

Flecainide

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8
Q

How do class IA, IB, and IC vary in their effects on the Na+ channel?

A

IB are weakest
IC are intermediate
IA are most potent

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9
Q

What’s one class II drug (aka beta blocker) used for arrhythmias?

A

Atenolol

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10
Q

What’s one class III drug to remember?

A

Dofetilide (specific K+ channel inhibitor)

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11
Q

What’s one class IV drug (aka. Ca++ blocker) to remember?

A

Verapamil

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12
Q

Aside from it’s effects on the Na/K pump, how can digoxin affect arrhythmias?

A

It’s a muscarinic agonist as well.

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13
Q

What Singh-Vaughan Williams classes of drugs can be used to treat V Tach?

A

Class I - Na+ blockers
Class III - K+ blockers
(both slowing conduction/decreasing excitability AND prolonging refractoriness counteract V Tach)

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14
Q

What Singh-Vaughan Williams classes of drugs can be used to treat A Fib?

A

Class I - Na+ blockers
Class III - K+ blockers
(both slowing conduction/decreasing excitability AND prolonging refractoriness counteract A Fib)

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15
Q

What Singh-Vaughan Williams classes of drugs can be used to treat AV reentry?

A

Class I - Na+ blockers
Class II - beta blockers
Class III - K+ blockers

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16
Q

What Singh-Vaughan Williams classes of drugs can be used to treat AV nodal reentry?

A

Class II - beta blockers
Class IV - Ca++ blockers
Others: digoxin and adenosine

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17
Q

What 3 parameters can you modify with drugs to affect reentrant tachycardias?

A

Excitability (class I), conduction velocity (class I), and effective refractory period (class III)

18
Q

What parameter can you modify with drugs to affect automaticity?

A

Phase 4 depolarization

19
Q

Which parameter is modified by drugs that predispose to tachycardias due to early afterdepolarizations?

A

Prolonged action potential duration.

Class III drugs, i.e. K+ blockers, do this… and thus predispose to Torsade des pointes

20
Q

How does HR modify the effect of Na+ channel blockade?

A

Faster HR -> the drugs block the channels more.

21
Q

How does membrane potential affect the ability of Class I drugs to block Na+ channels? How is this relevant to choosing a drug in ischemia-related arrhythmia?

A

More depolarized -> easier to block.
In ischemia, myocytes are more depolarized.
Lidocaine, being class IB and less potent, will thus selectively block Na+ channels in ischemic myocytes.

22
Q

3 parameters that increase the potency of K+ blockers in prolonging action potential duration (APD)?

A

Slow HR
Low extracellular K+ (makes sense. If there’s less K+, blocking it’s movement will have greater relative effect)
Low extracellular Mg++

23
Q

What 2 ions do you want to target when dealing with arrhythmia caused by “fast response” tissue i.e. myocytes & His-Purkinje system?

A

Na+ and K+

Thus, Class I and Class III drugs.

24
Q

What 4 surface molecules can you target when trying to deal with arrhythmias generated by “slow response” tissue i.e. SA and AV nodes?

A 
Beta receptors (causes decreased Ca++ current - I(Ca) )
Ca++ channels
Muscarinic receptors (decreased I(Ca), increased I(KAch) )
Adenosine receptors (decreased I(Ca), increased I(KAch) )
25
Q

Class II, Class IV, digoxin, and adenosine all have what effect on SA rate, AV node ERP, and AV node excitability?

A

All decrease SA rate
Increase AV node effective refractory period
Decrease AV node excitability

26
Q

If you want to prolong ERP in fast response tissue, what do you use?
In slow response tissue?

A

Fast response: block K+

Slow response: block Ca++ (or other drugs that indirectly lower Ca++)

27
Q

Do drugs distinguish between cardiac and vascular smooth muscle Ca++ channels?

A

Yep.

28
Q

What’s a Ca++ blocker specific for cardiac Ca++ channels?

A

Verapamil

29
Q

What’s a Ca++ channel blocker specific to vascular smooth muscle Ca++ channels? (what would this do?)

A

Nifedipine (this drug dilates blood vessels -> rapid and dramatic drops in SVR and BP)

30
Q

What’s a Ca++ blocker that affects both cardiac tissues and vascular smooth muscle?

A

Diltiazem

31
Q

What drug would you give to most rapidly address a tachycardia caused by slow response tissue?

A

Adenosine

people used to give IV Varapamil

32
Q

Would a K+ blocker better address a reentry tachycardia with a “short” or “long” excitability gap?

A

Class IA and III drugs work for short excitability gaps (I guess they can… get rid of them completely, stopping the reentry circuit).
They don’t work if the excitability gap is too long.

33
Q

Can class I drugs cause reentry to get started?

A

Yes, by making the slow path slower.

34
Q

(This lecture doesn’t have much internal consistency…) Can you also target the AV node (with beta blockers, Ca++ blockers, digoxin, adenosine) to treat AVRT?

A

Apparently. (wasn’t mentioned earlier… apparently you can use any of these antiarrhythmia drugs for AVRT???)

35
Q

You’ve got someone in AVRT and you give them sotolol (class III + beta blocker). This fixes the arrhythmia, with an initial disappearance of the P wave. Where did the block occur?

A

The block occurred in the bypass tract - the conduction couldn’t get back up to the atria to cause atrial depolarization (P wave).

36
Q

You’ve got someone in AVRT and you give them esmolol (beta blocker). This fixes the arrhythmia - it ends on a P wave that isn’t followed by a QRS. Where did the block occur?

A

The block occurred at the AV node.

37
Q

Can you treat post-MI ventricular tachycardia with lidocaine?

A

No, you need a more potent Na++ blocker.

surviving fibers aren’t necessarily ischemic, but they’re slow because of reduced gap junctions -> reentry circuit

38
Q

What classes of drugs CAN’T you use for AVNRT?

A

Class I and III.
You want to target the slow response tissue of the AV node… using beta blockers (class II), Ca++ blockers (class IV), digoxin, or adenosine.
(IV verapamil or adenosine for acute, others for prevention)

39
Q

2 factors predisposing for A Fib? (there are probably others)
Why?

A

It’s all about the wavelets: allow them more room, or make the wavelengths smaller.
Enlarged atria. (more area -> more possibility for wavelet microcircuits)
Alcohol -> shortens effective refractory period -> shortened wavelength.

40
Q

What’s the equation for electrical wavelength (relevant to A fib)?

A

Wavelength = ERP * conduction velocity

41
Q

What are 2 places you target when treating A Fib? Drugs that do this?

A 
The atria - prolong the ERP so the wavelets don't fit. (class I and III)
The AV node - prolong the ERP so fewer impulses are transmitted. (class II, IV, digoxin)
42
Q

Treatment for Torsade des pointes?

A

Remove IA and III drugs.
Give isoproterenol to increase HR.
Pacing.

43
Q

4 conditions that raise risk of using anti-arrhythmia drugs?

A 
Long QT (genetic, low K+ or Mg++)
Sick sinus syndrome (SA node too slow)
AV block
Poor systolic function
(you should be able to figure out which drugs make which worse)

Cardiology (46 decks)

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